The role of aldosterone and aldosterone-receptor antagonists in heart failure.

Prolonged overactivation of neurohormonal mechanisms in heart failure produces deleterious effects on the cardiovascular system and leads to poor prognosis. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers have been shown to interrupt this excessive overactivity and improve survival. Activation of the renin-angiotensin system leads to increased synthesis of aldosterone in heart failure. Some aldosterone production is independent of ACEs; therefore, ACE inhibition does not entirely suppress the excessive formation of aldosterone. An excess of aldosterone in heart failure leads to sodium retention and myocardial fibrosis. The use of aldosterone antagonists, combined with standard therapy for heart failure, improves morbidity and mortality.